Term
| EPI, NE, & ISO D/R Plots w/& w/out Antagonists (Bronchial Smooth muscle) |
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Definition
ISO=ISO + PHENTOLAMINE>>>>ISO + PROPRANOLOL
**ISO = NONSELECTIVE BETA AGONIST & PHENT= ALPHA ANTAGONIST; THERE WILL BE NO SHIFT IN THE D/R PLOT WHEN PHENT ADDED W/ISO SINCE BRONCHIAL SMOOTH MUSCLE CONTAINS NO ALPHA RECEPTORS ANYWAYS!
THERE WILL BE A SHIFT TO THE RIGHT ON THE D/R PLOT WHEN PROP ADDED, SINCE PROP WILL ANTAGONIZE ISO @ THE BETA RECEPTORS OF BRONCHIAL S.M., SO YOU WILL NEED MORE DOSE OF ISO TO GET SAME RESPONSE WHEN YOU ADD PROP! |
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Term
| EPI, NE, & ISO D/R plots w/& w/out antagonists (Cardiac inotropism) |
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Definition
NE=NE + phentolamine >>>>NE + Propranolol
**THERE WILL BE NO SHIFT WHEN PHENT (ALPHA ANTAG) ADDED W/NE BECAUSE HEART HAS BETA-1 RECEPTORS, NO ALPHA RECEPTORS
THERE IS A SHIFT TO THE RIGHT WHEN PROP (BETA BLOCKER) ADDED, BECAUSE IT WILL ANTAGONIZE EFFECTS OF NE AND YOU WILL THEREFORE NEED A BIGGER DOSE TO PRODUCE SAME RESPONSE |
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Term
| WHY NO REFLEX TACHYCARDIA WHEN PHENTOLAMINE ADMINISTERED IN VITRO? |
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Definition
| IN VITRO MEANS NO REFLEX RESPONSES!!! IF IT WAS IN VIVO, THERE WILL BE REFLEX TACHY SINCE ALPHA ANTAG WILL CAUSE DECREASED PERIPHERAL RESISTANCE AND HYPOTENSION |
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Term
| What affects cardiac ionotropism? |
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Definition
| cardiac ionotropism has to do with force of contraction, so beta 1 receptor stimulation will have some effect |
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Term
| EPI + PROP (arterial smooth muscle)--what is the D/R plot going to look like? |
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Definition
| epi is much more potent than NE, so you will need a smaller dose; now if we put epi with prop, there will be no shift because prop is a beta blocker, and arterial smooth muscle contractility is an alpha mediated response |
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Term
| EPI + Phentolamine (arterial smooth muscle)--what is the D/R plot going to look like? |
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Definition
| since PHENTOLAMINE IS AN ALPHA ANTAGONIST, THERE WILL BE A RIGHTWARD SHIFT IN THE D/R PLOT FOR EPI. |
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Term
| How does denervation affect an agonist's efficacy (2 ways) |
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Definition
agonist will produce a greater response:
1). reuptake sites are lost (reuptake most important factor)
2). receptor up-regulation occurs (this happens later on) |
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Term
| How does denervation affect receptors on skeletal muscle? |
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Definition
| in the case of skeletal muscle, there will be an increase in the # of receptors and binding sites on the neuromuscular endplate |
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Term
| what happens to I.A.S. when there's denervation? |
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Definition
| response to i.a.s. is diminished or abolished because an intact neuron is needed for the i.a.s. to produce effect |
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Term
| How do adrenergic neuron blockers affect activity of catecholamine after it's administered? |
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Definition
| since adrenergic neuron blockers lessen the release of catecholamines from the adrenergic nerve, there will be a slight increase in response to an administered catecholamine because the receptors will have upregulated post junctionally |
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Term
| how does an adrenergic neuron blocker affect i.a.s.? |
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Definition
| an adrenergic blocker lessens the amount of NE being released, so i.a.s. will have little effect since i.a.s. works by promoting release of NE from adrenergic neuron |
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Term
| How does reuptake inhibition affect administration of catecholamine? |
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Definition
| pretreatment w/reuptake inhibitor will increase the catecholamine response because it's not being taken up into the adrenergic nerve |
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Term
| How does reuptake inhibition affect response of I.A.S. |
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Definition
| since i.a.s. needs to be taken up into the adrenergic nerve to have an effect, reuptake inhibition will decrease/abolish response to i.a.s. |
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Term
| Can reuptake inhibition cause downregulation? |
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Definition
| with chronic use of reuptake inhibitor, yes. (example--chronic cocaine use) |
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Term
| where is an i.a.s. taken up in the adrenergic nerve? |
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Definition
| at the nerve terminal ending |
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Term
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Definition
| acts on alpha receptors of arterioles to produce vasoconstriction and reflex bradycardia |
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Term
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Definition
| acts on h1 receptors of arterioles to produce vasodilation and reflex tachycardia |
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Term
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Definition
| nonselective, competitive alpha antagonist; abolishes increase in b.p. by phenylephrine; prevents reflex bradycardia, but can produce reflex tachycardia depending on amount of agonist activity going on (more reflex tachy if standing up opposed to lying down) |
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Term
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Definition
| h1 antagonist; prevents histamine reflex response (reflex tachy); will not have much effect on blood pressure because histamine not released chronically to maintain b.p. and in order for antagonist to work, agonist must be present (h1 receptors are naked!) |
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Term
| alpha agonist and sympathetic neuron firing |
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Definition
| alpha agonist will decrease firing because there is reflex bradycardia going on (reflex decrease in symp stimulation) |
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Term
| histamine and sympathetic neuron firing |
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Definition
| increases firing because histamine agonist activity produces reflex tachycardia (reflex increase in symp stimulation) |
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Term
| how do you describe neuron firing? |
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Definition
| a neuron is firing when it's releasing NE |
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Term
| alpha agonist and vagal nerve activity/H.R. |
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Definition
| alpha agonist increases vagal firing due to reflex bradycardia (reflex increase in vagal stimulation); H.R. is decreased |
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Term
| histamine and vagal nerve activity/H.R. |
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Definition
| histamine will reduce vagal firing because of reflex tachycardia; histamine increase H.R. |
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Term
| epinephrine metabolic effects |
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Definition
increased lactate in muscle
increased FFA
increased glucose
inhibition of insulin release (via alpha-2 interaction)
increase glucagon release (via beta 2 interaction)
increases adenyl cyclase and cAMP
liver/muscle increases phosphorylase
glycogenolysis; G-1-P, G-6-P
increases adipose TG lipase to form FFA |
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Term
| alpha agonist--noncatecholamines (synthetic) |
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Definition
phenylephrine (prototype)
methoxamine
metaraminol
mephentermine
**first 3 mostly asked on exams |
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Term
| beta-2 agonists--noncatecholamines |
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Definition
ritodrine (yutopar)
metaproterenol (metaprel)
terbutaline (bricanyl)
albuterol (ventolin) levalbuterol (xopenex)
salmeterol xenofoate (serevent)
formoterol (foradil) |
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Term
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Definition
bronchodilation--think asthma
premature labor--uterus has beta 2 receptors that upon stimulation by beta 2 agonist will "quiet down" (relax) uterus |
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Term
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Definition
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Term
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Definition
| for acute asthma (asthma attacks); can produce down regulation with long term use |
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Term
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Definition
| for acute asthma (asthma attacks); can produce down regulation with long term use |
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Term
| salmeterol xenofoate (serevent) |
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Definition
| long acting agent for asthma; prevents down regulation, but not for asthma attacks |
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Term
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Definition
| long acting asthmatic agent that is not used for asthma attacks; prevents down regulatioin |
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Term
| type a effects of beta 2 agonists |
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Definition
| cardiac effects (beta 1 effects) |
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Term
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Definition
ephedrine (mixed action)
tyramine (peripheral acting)
amphetamine
methamphetamine |
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